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This work examines the individual and comprehensive effects of oxytocin, maternal depression, and breastfeeding on the mother-infant bond. Self-report measures are used to illustrate differences in behavior, temperament, and maternal feelings towards her infant and her experiences associated with motherhood. Based on previous literature highlighting the protective and beneficial effects of oxytocin during maternity, results from this longitudinal study examining mother-infant dyads from prenatal to three-months postpartum are aimed to combine psycho-social and biological components associated with child rearing to form a complete understanding of the mother-infant bonding system. While our research provides support for certain psycho social components by demonstrating an irrefutable impact of depressive symptoms and breastfeeding self-efficacy on later displays of postpartum attachment, there is still room for question in regards to the role that oxytocin may play. / Includes bibliography. / Thesis (M.A.)--Florida Atlantic University, 2019. / FAU Electronic Theses and Dissertations Collection

Background. Social deprivation or isolation accelerates the progression of atherosclerosis in several animal models of the disease. Conversely, stable social environment has been associated with reduction in the extent and severity of atherosclerosis. While positive social interactions are thought to be related to this protective effect, little is known about the physiological mechanisms responsible. Recently, the neurohypophyseal peptide, oxytocin (OT), has been found to play a role in both positive social interactions and cardiovascular homeostasis, suggesting that this neuropeptide may be responsible for mediating the beneficial effects of positive social environment on atherosclerosis. The first aim of the current study is to examine the potential anti-inflammatory effects of OT on in vitro cellular models involved in the pathophysiology of atherosclerosis. The second aim is to examine whether long-term administration of OT slows the progression of atherosclerosis in apoE-/- mice. The third aim is to obtain evidence in vivo that OT is impacting disease through novel anti-inflammatory effects on tissues important in atherogenesis. Methods. 1) Human macrophage-like (DTHP-1) cells and human aortic endothelial cells (HAECs) were stimulated with lipopolysaccharde (LPS) alone, and in the presence of different concentrations of OT, and IL-6 secretion was measured. 2) ApoE-/- mice were socially isolated at 12 weeks of age and continuously infused with OT (n=24) or vehicle (n=21) from subcutaneously implanted osmotic minipumps for 12 weeks. Plasma levels of lipids, adiponectin, insulin, and CRP were assessed pre- and post-treatment. Extent of aortic atherosclerosis (percent lesion area) was assessed post-treatment and areas of high lesion prevalence were compared between OT and vehicle (VH) control groups. Constitutive release of IL-6 from ex vivo adipose tissue samples taken from a subset (n=12/group) was compared between treatment groups. Results. 1) OT demonstrated dose-dependent inhibition of LPS-induced IL-6 secretion from macrophages (35-55%, p < 0.01) and aortic endothelial cells (15-25%, p < 0.01). 2) ApoE-/- mice continuously infused with OT displayed decreased plasma CRP levels after 6 weeks of treatment and diminished lesion area at the thoracic aorta after 12 weeks of treatment relative to vehicle control animals (37%, p < 0.05). Additionally, adipose tissue samples taken from OT infused mice showed decreased constitutive release of IL-6 (30%, p < 0.01). These findings were unrelated to changes in plasma lipids, insulin, physical activity levels, or 24-hour corticosterone secretion. Discussion and Conclusions. These findings demonstrate that OT is capable of inhibiting stimulated pro-inflammatory cytokine production in macrophages and aortic endothelial cells in vitro, and constitutive release from adipose tissue in vivo. OT also decreased circulating CRP levels and slowed the progression of early stage atherosclerosis in an aortic region of high lesion prevalence in socially isolated apoE-/- mice. Taken together, these results suggest that increased peripheral OT could be partially responsible for the beneficial effect of positive social environment on atherosclerosis.

Social support has been demonstrated to reduce cardiovascular disease morbidity and mortality; however, the mechanisms by which social support reduces disease progression are still unclear. Oxytocin (OT) is a neuropeptide commonly associated with positive social interactions. This series of studies investigated the ability of oxytocin to attenuate atherosclerosis and its putative mediators, pro-inflammatory cytokines. Oxytocin receptors were identified by Western Blot on rat adipose tissue and rat adipocytes. OT receptor mRNA was identified in human adipocyte cDNA. In primary culture of rat abdominal adipocytes, oxytocin (10 pM) decreased LPS-induced IL-6 release by 24.9% after a six hour incubation. Adipose tissue, surgically dissected from ApoE-/- mice chronically infused with OT, secreted less IL-6 than mice infused with a vehicle control. In sum, the presence of OT receptors was demonstrated on adipocytes, OT was shown to reduce IL-6 release in vitro, and chronic OT infusion decreased IL-6 release in adipose explants immediately after sacrifice. Potential mechanisms by which adipose tissue's role in the sympathetic nervous system response may affect inflammation, metabolism, and disease are discussed.

The pre-pubertal infancy stage of development is marked by numerous neurological and behavioral changes in Syrian Golden Hamsters. One of the most notable changes during this period is the onset of social behaviors including social playfighting. Social playfighting is initiated approximately two weeks postpartum and is completely abolished by mid-puberty. The neural mechanisms that underlie this behavioral change are not well understood, but previous research has identified both oxytocin (OT) and serotonin (5-HT) as possible regulators of this behavior. In the present study, immunohistochemical techniques were used to evaluate changing levels of OT and serotonin 5-HT in the developing brain with the hypothesis that both OT and 5-HT levels would increase and decrease simultaneously with the onset and decline of social playfighting. Additionally, it was predicted that injections of a 5-HT3 receptor agonist, m-Chlorophenylbiguanide hydrochloride (CBG), into hamster in late infancy would reinstated social playfighting behaviors. Contrary to the hypothesis, OT was found to continually increase in the fornix, lateral hypothalamus, nucleus accumbens, medial preoptic area, and anterior hypothalamus, while 5-HT continually decreased in the lateral septal nucleus and medial preoptic area. CBG injections did not reinstate social playfighting behaviors, however a large stress effect was observed, potentially masking any other effect. Analysis of OT and 5-HT receptors during this developmental stage is necessary for a better understanding of this neural mechanism. Further research into this topic may have important implications for animal models of autism spectrum disorders. / text

Thesis (M.S.)--Virginia Polytechnic Institute. / Also available via the Internet.

Thesis (M. Sc. (Pharmacy)) - Rhodes University, 2007.

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Background: In spite of the importance of maternal sensitivity as a construct that fosters secure attachment and promotes a child’s social and cognitive development, no routine clinical screening currently identifies mothers at risk of poor maternal sensitivity. This is partly because researchers have not identified all the factors that influence maternal sensitivity. As a result, parenting interventions to promote maternal sensitivity and optimise child outcomes tend to focus on clinical groups. Thus, more attention is needed to identify possible determinant factors. The neurobiological mechanisms underlying natural variation in maternal sensitivity (i.e. sensitive and less sensitive mothers) are poorly understood, especially the putative role of the hormone Oxytocin (OT). Literature has suggested that this variation in maternal sensitivity is an outcome of interaction between maternal OT, as well as social factors (e.g. perceived parenting) and this interaction charts the discrete profile of the maternal brain that is mediated by stress- and reward-related neural systems. To date no study examined for the neurobiological correlates of maternal sensitivity in a distinct group of mothers representing natural variations in maternal sensitivity. Methods: Out of 105 women recruited from community antenatal clinics during their pregnancy, to complete a set of self-reported questionnaires assessing their psychosocial characteristics, a total of 80 new (i.e. early postpartum) mothers and their infants were followed up and underwent evaluation of maternal sensitivity at 4-6 months postpartum. Using a stepwise regression, we examined for predictors of maternal sensitivity among the sample (Study I). Later, at 7-9 months postpartum, 30 mothers, representing extremes in maternal sensitivity, were selected from this sample of 80: 15 mothers with higher scores (high sensitivity mothers - HSMs), and 15 with lower scores for maternal sensitivity (low sensitivity mothers - LSMs), underwent functional Magnetic Resonance Imaging (fMRI) to examine their brain responses when viewing videos of their own and an unknown infant. Maternal plasma OT levels were also measured before and following an interactive play with their infant (Study II). Results: Mothers’ self-reported experience of own parental care, and household income, independently predicted maternal sensitivity, accounting for 17% of the variance. Comparing mothers grouped by maternal sensitivity level, HSMs showed a drop in their plasma OT levels following the interaction with their infant. HSMs also showed significant brain activation in the right superior temporal gyrus in response to own infant (compared to unknown infant) when compared to LSMs. By contrast LSMs did not show any change in their plasma OT levels following interaction with their infant, and their brain responses to own infant did not show any significant brain activation when compared to HSMs. Conclusions: The findings may have implications for future novel approaches for early assessment of mothers at risk of low maternal sensitivity so they could be targeted by specialised assessments and consequently interventions to improve their parenting (Study I). Maternal sensitivity is accompanied by neural correlates that could act as a biomarker for future intervention studies that target vulnerable mothers (Study II).